Sclerotinia stem rot in soybean, also know as white mold, is caused by the fungus pathogen Sclerotinia sclerotiorum. The disease was first reported in Hungary in 1924, and has since been reported in many other countries, including the USA. The disease has become increasingly important in the USA since 1990. For example, Sclerotinia stem rot caused an estimated yield loss of 6.4×105 metric tons in the USA during 1994 (Wrether et al. (1997) Plant Dis 81:107-110). Yield has been shown to be inversely correlated with the percent incidence of Sclerotinia stem rot. Yield loss has been estimated at 250 kg/ha for each 10% increment in diseased plants (Grau and Hartman (1999) Compendium of Soybean Diseases, 4th ed. APS Press, St. Paul, Minn., USA, pp. 46-48).
S. sclerotiotum infects soybean plants in the form of ascospores that land on flowers (Grau (1988) Am Phytopathol Soc, St. Paul, Minn., USA pp 56-66). The ascospores germinate under adequate moisture condition and use the flower petals as a nutrient base. Stem lesions originate at leaf axils where flowers are positioned and advance up and down the stem. Symptoms of the Sclerotinia stem rot begin to develop at growth stages R2 and R3. Lesions are most frequently on the main stem and completely encircle the stem and disrupt the transport of water, mineral nutrients, and photosynthates to developing pods. Pod development and pod fill above stem lesions are reduced, resulting in yield reduction.
Soybean genotypes show large variations in resistance to Sclerotinia stem rot (Kim et al. (1999) Crop Sci 39:64-68). So far, no soybean genotypes with complete resistance to S. sclerotiorum have been identified. The heritability of partial resistance, measured with a disease severity index (DSI), was estimated to be 0.59 with significant genotype and environment interaction observed (Kim and Diers (2000)Crop Sci 40:55-61). Quantitative trait loci (“QTL”) analysis identified three QTL explaining 10, 9, and 8% of the variability for DSI across environments and locating on linkage groups C2, K, and M. Two of the QTLs were also significantly associated with disease escape mechanisms such as plant height, and date of flowering.
Breeding for white mold resistance via the traditional approach has been very difficult, due to the multigenic nature of this trait. What is needed in the art is a means to identify genes conferring resistance to white mold, using molecular markers. These markers can then be used to tag the favorable alleles of these genes in segregating dicot populations and then employed to make selection for resistance more effective. The present invention provides this and other advantages.